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Tumor necrosis factor-α promotes the expression of excitatory amino-acid transporter 2 in astrocytes: Optimal concentration and incubation time

The aim of the present study was to determine whether tumor necrosis factor (TNF)-α regulates the expression levels of excitatory amino-acid transporters (EAATs) in primary astrocytes and its roles in brain ischemia. Exogenous TNF-α was administered to pure cultured astrocytes and the expression lev...

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Detalles Bibliográficos
Autores principales: DING, YUEMIN, ZHANG, KENA, LIU, SHUQIN, ZHANG, QIJUN, MA, CHIYUAN, BRUCE, IAIN C., ZHANG, XIONG
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4217772/
https://www.ncbi.nlm.nih.gov/pubmed/25371754
http://dx.doi.org/10.3892/etm.2014.2024
Descripción
Sumario:The aim of the present study was to determine whether tumor necrosis factor (TNF)-α regulates the expression levels of excitatory amino-acid transporters (EAATs) in primary astrocytes and its roles in brain ischemia. Exogenous TNF-α was administered to pure cultured astrocytes and the expression levels of EAAT1, EAAT2 and glial fibrillary acidic protein (GFAP) were evaluated. The results showed that TNF-α at 10 ng/ml enhanced the expression of EAAT2 in a time-dependent manner, while the expression levels of EAAT1 and GFAP did not change. To determine whether the elevation in the levels of the EAAT2 protein induced by TNF-α had a beneficial effect on ischemic insult, TNF-α was applied to in vitro models of cerebral ischemia; the treatment was observed to increase neuronal viability. The present results suggest that a relatively short-term application of an optimal concentration of TNF-α may protect neurons against ischemic injury by elevating the expression of EAAT2 in astrocytes.